LC is a poorly absorbed, well-tolerated, and efficient phosphate binder. LC-treated dialysis patients show almost no evolution toward low bone turnover over one year (unlike CC-treated patients), nor do they experience any aluminum-like effects on bone.
Background. The evidence base regarding the safety of intravenous (IV) iron therapy in patients with chronic kidney disease (CKD) is incomplete and largely based on small studies of relatively short duration. Methods. FIND-CKD (ClinicalTrials.gov number NCT00994318) was a 1-year, open-label, multicenter, prospective study of patients with nondialysis-dependent CKD, anemia and iron deficiency randomized (1:1:2) to IV ferric carboxymaltose (FCM), targeting higher (400–600 µg/L) or lower (100–200 µg/L) ferritin, or oral iron. A post hoc analysis of adverse event rates per 100 patient-years was performed to assess the safety of FCM versus oral iron over an extended period. Results. The safety population included 616 patients. The incidence of one or more adverse events was 91.0, 100.0 and 105.0 per 100 patient-years in the high ferritin FCM, low ferritin FCM and oral iron groups, respectively. The incidence of adverse events with a suspected relation to study drug was 15.9, 17.8 and 36.7 per 100 patient-years in the three groups; for serious adverse events, the incidence was 28.2, 27.9 and 24.3 per 100 patient-years. The incidence of cardiac disorders and infections was similar between groups. At least one ferritin level ≥800 µg/L occurred in 26.6% of high ferritin FCM patients, with no associated increase in adverse events. No patient with ferritin ≥800 µg/L discontinued the study drug due to adverse events. Estimated glomerular filtration rate remained the stable in all groups. Conclusions. These results further support the conclusion that correction of iron deficiency anemia with IV FCM is safe in patients with nondialysis-dependent CKD.
Objective To examine the effect of a reduced calcium/magnesium dialysis fluid (1.25/0.25 mmol/L, respectively) on calcium and magnesium mass transfer in both 1.36% and 3.86% glucose solutions. Design Each patient underwent four test exchanges, two with a standard dialysis fluid containing 1.36% and 3.86% glucose, and two with a reduced calcium/magnesium fluid containing 1.36% and 3.86% glucose. Calcium and magnesium were measured in dialysate and serum at ° and 240 minutes. Setting Single renal unit of a university teaching hospital. Patients Sixteen patients established on CAPD, and peritonitis-free, for at least 3 months. Results A lower dialysate calcium results in negative mass transfer when serum-ionized calcium exceeds dialysate calcium (mean -.0.21±0.15 mmol/exchange), and positive mass transfer when serum-ionized calcium is less than dialysate calcium in 1.36% glucose solutions (mean 0.57±0.18 mmol/exchange). A negative correlation was found between serum-ionized calcium level and calcium mass transfer. With a 3.86% reduced calcium/magnesium solution, calcium mass transfer is always negative (-.0.88±0.18 mmol/exchange) due to ultrafiltration and solute drag. Fifteen patients were found to be hypermagnesemic at the time of the study. Magnesium mass transfer was neutral with the standard 1.36% glucose fluid (mean -.0.01 mmol/exchange), but negative with the reduced calcium/magnesium 1.36% glucose fluid (mean -.0.58±0.13 mmol/exchange). With the 3.86% glucose solution, both fluids produced negative magnesium mass transfer (mean -.0.32±0.11 and -1.07±0.11 mmol/exchange for standard and reduced calcium/magnesium fluids, respectively). Conclusions We conclude that this fluid formulation should reduce hypercalcemia and hypermagnesemia in CAPD patients.
Patients with chronic kidney disease have a high burden of cardiovascular morbidity and mortality. The vast majority of patients with chronic kidney disease do not progress to end stage renal failure, but do have a significantly higher incidence of all cardiovascular co-morbidities. Traditional cardiovascular risk factors only partially account for this increased incidence of cardiovascular disease. In patients with kidney disease the basic biology underlying cardiovascular disease may be similar to that in patients without kidney disease, but it would seem many more risk factors are involved as a consequence of renal dysfunction. Although emphasis is placed on delaying the progression of chronic kidney disease, it must be appreciated that for many patients it is vital to address their cardiovascular risk factors at an early stage to prevent premature cardiovascular death. This review examines available epidemiological evidence, discusses common cardiovascular risk factors in patients with chronic kidney disease, and suggests possible treatment strategies. Potential areas for important research are also described.
Patients with recurrent laryngeal nerve (RLN) paresis demonstrate impaired function of laryngeal muscles and swallowing. The cricopharyngeus muscle (CPM) is a major component of the upper esophageal sphincter. It was hypothesized that the RLN innervates this muscle. A nerve branch leading from the RLN to the CPM was found in adult sheep by anatomic dissection. Electrical stimulation of the RLN elicited a muscle action potential recorded by electrodes placed in the ipsilateral CPM. Swallowing was investigated by mechanical stimulation of oropharynx pre- and postsectioning of the RLN. Severing of the RLN resulted in a loss of the early phases of swallow-related CPM electromyographic activity; however, late-phase CPM electromyographic activity persisted. The RLN provides motor innervation of the CPM, which also has innervation from the pharyngeal plexus.
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